Letter Taenia solium and neurocysticercosis
MJA 2001; 175: 670-671
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To the Editor: A 37-year-old Australian-born white woman presented
on Christmas eve with a focal seizure with secondary generalisation.
This had developed on a background of bifrontal headaches for which
she had been taking ibuprofen. She was in otherwise good health, with
no previous history of seizures, head injury or meningitis. On
examination there were no focal neurological signs. Fundoscopy
findings were normal. Computed tomography (CT) of the brain showed a
small contrast-enhancing lesion, radiologically suggestive of a
brain tumour. Therapy with phenytoin and dexamethasone was started,
and she was referred for neurosurgical assessment. A magnetic
resonance imaging (MRI) scan showed an 8 x 12 mm-enhancing nodule in
the right posterior frontal cortex with surrounding oedema
(Figure). She underwent excisional biopsy of the lesion, and
histopathological examination showed a cysticercus cyst, the
encysted larval form of Taenia solium, associated with an
intense surrounding inflammatory reaction. Further questioning of
the patient revealed that she was a frequent visitor to South-East
Asia, where this organism is endemic in some areas.1,2 She remains
well and seizure-free at follow-up.
T. solium (pork tapeworm) is associated with two distinct infective states in humans: asymptomatic intestinal infection by an adult tapeworm, and cysticercosis, which is associated with clinical disease. Ingestion of eggs in contaminated food or water by an intermediate host, typically pigs but sometimes humans, leads to the development of cysticercosis, as seen in our patient. Humans acquire intestinal infection with the adult tapeworm by ingesting encysted larvae (cysticerci) in undercooked meat.1-3 Epilepsy is the most common presentation.1,2,4 The findings of cysticerci outside the central nervous system (such as in the posterior chamber of the eye, palpable within subcutaneous tissues, or as calcified nodules on plain x-rays) and the detection of anticysticercal antibodies in plasma or cerebrospinal fluid may assist in diagnosis of neurocysticercosis, and subsequently prevent unnecessary neurosurgery. However, patients with a single cerebral lesion or those with only calcified lesions are commonly seronegative.1-3 Stool examination for tapeworm eggs is insensitive, but may identify patients with intestinal infection.2 Whether treatment with praziquantel or albendazole improves long term outcome remains controversial.2,5 In cases of encephalitis, subarachnoid, spinal or ocular involvement, symptoms may worsen secondary to an inflammatory reaction around degenerating cysts. Co-administration of corticosteroids ameliorates some of this effect. Surgical treatment is reserved for patients with hydrocephalus.1-3 Neurocysticercosis is uncommon in Australia.5 Our case reminds us of the risks of infective diseases posed to travellers and migrants. It also highlights the importance of considering infective causes such as cysticerci, bacterial abscesses, toxoplasmosis and cryptococcomas in the differential diagnosis of space-occupying lesions seen on central nervous system imaging. Anthony T Zimmermann,* William S Jeffries
©MJA 2001
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